1. Field of the Invention
The present invention relates to a semiconductor device and operation method thereof, and more particularly to a synaptic semiconductor device and operation method thereof.
2. Description of the Related Art
The nervous system of a living body is consisted of numerous nerve cell neurons and synapses connecting neurons. Synapses may be classified as electrical or chemical, based on the signal transmission between neurons. The electrical synapses are found in invertebrates and myocardial cells etc. Since the others are known as the chemical synapses, hereinafter, word of “synapse(s)” indicates the chemical synapse(s).
Recently, many studies have been made to mimic the nervous system of a living body, in particular the brain nervous system, by a nerve-like circuit system (i.e., a neuromorphic computation system) using semiconductor devices.
By the way, in order to embody the neuromorphic computation system, the following properties of the nervous system of a living body must be considered.
First, a short-term memory is biologically formed of synaptic connections or a potentiation of the synaptic connections and a long-term memory is composed of the growth of new synapses etc. in the stimulated place through gene expression in the nucleus of a neuron by repetitive stimulation. This content refers to pp. 293-308 of a Korean translated book of ‘In Search of Memory’ by Eric R. Kandel, which is translated by Deaho Jeon and published by Random House Korea Inc. in 2011 (Reference 1). FIGS. 1 and 2 are redrawn from Reference 1.
In order to analyze a transition mechanism from a short-term memory to a long-term memory, Kandel, the original author of Reference 1, performed the experiment of learning (memory) of stimulation in Aplysia which has relatively a simple nervous system and obtained the results as shown in FIG. 1.
FIG. 1 is a simple drawing of a nervous system of Aplysia. According to (a) in FIG. 1, an external stimulation impacted on a tail 1 activates an interneuron releasing serotonin and the interneuron is connected to a sensory neuron connected to a siphon 2 and a motor neuron controlling a shrinking reflection of a gill 3, respectively.
In FIG. 1, (b) is an enlarged view of a part A in (a) for explaining a short-term memory mechanism when a single stimulation is applied. The neurotransmitter serotonin released from an interneuron is binding to a receptor of a sensory neuron and induces the increase of cyclic AMP and protein kinase A in the sensory neuron. Subsequently, vesicles having the neurotransmitter at the axon terminal of the sensory neuron are moved to a plasma membrane and burst to transmit the stimulated signal to the motor neuron. As a result, the stimulation remains in the short-term memory.
On the other hand, (c) in FIG. 1 is drawn to explain the mechanism of a long-term memory when repetitive stimulation is applied 5 times. The repetitive stimulation induces the repetitive release of serotonin from the interneuron. The released serotonin increases the amount of cyclic AMP in the sensory neuron, and then protein kinase A and MAP kinase move into the nucleus to activate CREB-1 and inactivate CREB-2 respectively for gene expression. Subsequently, the repetitive stimulation remains in the long-term memory through the change of cell functions or structures such as the growth of new synapses etc.
Thus, when the regular stimulation is repeatedly applied to a living body, according to the increase of cyclic AMP in a neuron, the short-term memory is transited to the long-term memory through the change of functions or structures of a synapse by gene expression in the nucleus of a neuron.
Additionally, as shown in FIG. 2, Kandel, the original author of Reference 1, insisted that in a cell culture system having a single sensory neuron connected to two motor neurons via two synapses, the gene expression in the nucleus only affect the single synapse receiving 5 times of serotonin injection (5 times of stimulation) for the growth of new synaptic terminals etc.
The author, as shown in the enlarged view of FIG. 2, explains the reasons that (1) the mRNA synthesized by the repetitive stimulation in the nucleus of a sensory neuron is delivered to all axon terminals in a resting state, (2) serotonin injected 5 times in a single terminal changes the recessive CPEB (Cyto-plasmic Polyadenylation Element Binding protein: the protein with the self-perpetuation as like as the prion) being in a recessive state in all terminals into the dominant CPEB, (3) the dominant CPEB changes the recessive CPEB into the dominant one, and (4) the dominant CPEB meets and activates the mRNA moving into each axon terminal and then the activated mRNA synthesizes the proteins for changing the structure such as a new synaptic terminal growth etc. Consequently, the portion of the stimulated synapse is transited to the long-term memory.
Additionally, in order to embody the neuromorphic computation system, another important property of the nervous system of a living body has to be considered. It is a Spike-Timing Dependent Plasticity (STDP) that the synaptic connectivity is dependent on the fire time difference between pre- and post-synaptic neurons.
According to FIG. 3, each neuron 100, 200 or 300 has basically a nucleus 110 in a cell body (a soma), and there are a plurality of dendrites 120 to receive a stimulated signal around the cell body and an axon 130 connected by an axon hillock 122 to transmit the stimulated signal to one side of the cell body.
The axon 130 generally has a length of about 10,000 times of diameter of the cell body, is wrapped with a plurality of myelin sheaths 132 interlaid with a node of Ranvier 134 and consists of axon collaterals 136 and axon terminals 138.
A synapse 400, as an enlarged view shown in FIG. 3, indicates a connecting region between two neurons, namely, a meeting region between an axon terminal of the pre-synaptic neuron 200 and a dendrite of the post-synaptic neuron 100 interlaid with the narrow space, as a synaptic cleft 402, of about 20 nm.
The transmission process of the synapse 400 is simply described as the followings with respected to the enlarged view shown in FIG. 3.
First, when a fire is triggered by a stimulation exceeded over the threshold (Vth, an about −55 mV) in the pre-synaptic neuron 200, the stimulation as an electrical signal is transmitted to the axon terminal through the axon with the repeat of depolarization and repolarization by alternately opening and closing sodium 202 and potassium (not shown) channels, respectively.
The stimulation transmitted to the axon terminal of the pre-synaptic neuron 200 opens a calcium channel 204 and allows an influx of Ca2+ ions into the plasma membrane through the calcium channel. The intracellular Ca2+ ions bind to vesicles 206 filled up the neurotransmitters 208 and cause the vesicles 206 to fuse into the plasma membrane for releasing the internal neurotransmitters 208 into the synaptic cleft 402. The released neurotransmitters 208 diffuse to flow across the synaptic cleft 402 and arrive at dendrite membranes of the post-synaptic neuron 100.
Here, the neurotransmitters 208 enable the stimulation transmitted from the pre-synaptic neuron 200 through two kinds of channels to chemically transmit into the post-synaptic neuron 100.
Exactly, one is a ligand-gated ion channel that uses the diffused neurotransmitter 208 as a ligand which directly binds to the ion channel. Namely, if the neurotransmitter 208 binds to Na+ channel 102, Na+ ion flows into the post-synaptic neuron 100 for contributing towards excitation and if the neurotransmitter 208 binds to K+ channel 104, K+ ion flows out of the post-synaptic neuron 100 for suppressing excitation.
The other is a G-protein coupled receptor 106 mediated ion channel that is activated by the diffused neurotransmitter 208 which directly binds to the G-protein coupled receptor 106 on the plasma membrane of a dendrite in the post-synaptic neuron 100. In this time, an alpha subunit of the G-protein coupled receptor 106 is dissociated and directly couples to the ion channel or indirectly couples to an effecter 108 on the inner membrane for operating this ion channel through an intracellular second messenger (not shown). In other words, if the second messenger couples to a Na+ gate 102, Na+ ion flows into the post-synaptic neuron 100 for contributing towards the excitation and if the second messenger couples to a K+ gate 104, K+ ion flows out from the post-synaptic neuron 100 for suppressing the excitation.
The intracellular Na+ ions flow in the dendrite membrane of the post-synaptic neuron 100 through the Na+ channels 102, diffuse across the cell body and then collect at the axon hillock 122. When the sum of the intracellular Na+ ions and the ions transmitted from other dendrites 120 induces the depolarization by more than the threshold membrane potential (Vth) at the axon hillock 122, a fire is produced as a spike signal shown in FIG. 4. The spike signal is an electrical signal for transmission of the stimulation by again repeating the depolarization and the repolarization along the axon 130 of the post-synaptic neuron 100.
In FIG. 3, the stimulation is transmitted from the pre-synaptic neuron 300 to two different dendrites 120 of the post-synaptic neuron 100 through two different synapses by two signals (a) and (b), respectively and can be fired when the sum (a+b) of two signals (a) and (b) is exceeded over the threshold (Vth) at the axon hillock 122 of the post-synaptic neuron.
In FIG. 4, when the membrane potential reaches the threshold (Vth, −55 mV) at the point {circle around (1)}, the membrane of the axon 130 of the post-synaptic neuron 100 opens the Na+ channels, which allow Na+ ion inflow to produce a fire by a sudden membrane potential rising and then, at the point {circle around (2)}, closes the Na+ channels and simultaneously opens the K+ channels, which allow K+ ion outflow to reduce the membrane potential until the K+ channels are closed at about −80 mV, and then maintains −70 mV of the resting (equilibrium) membrane potential by operations of Na+ pumps and K+ pumps.
By the above mentioned reasons, the first fire is mainly generated at the axon hillock 122 of the post-synaptic neuron 100 and the Na+ ions entered by the first fire are rapidly diffused by the myelin sheath 132 to depolarize the neighbor axon membrane. As a result, the spike waveform as shown in FIG. 4 is transmitted to the axon terminal.
Thus, as shown in FIG. 3, since a single neuron is connected to two or more neurons through the different synapses in the real nervous system of a living body, in order to embody a neuromorphic computation system, it is important element that consideration of different fire times between pre- and post-neurons of a predetermined synapse. In other words, as shown in FIG. 3, when a fire is generated at an axon hillock 122 of a neuron 100, it is considered that the synaptic connectivity is potentiated in the synapses connected to a pre-fired neuron 200 or 300 and the synaptic connectivity is depressed in the other synapses.
Among prior research results to mimic the nervous system of a living body by considering the above mentioned properties, there are S. H. Jo, et al., Nanoscale Memristor Device as Synapse in Neuromorphic Systems, Nano Letters 10 (4), pp. 1297-1301, 2010 (hereinafter, Reference 2) and D. Kuzum, et al., Energy Efficient Programming of Nanoelectronic Synaptic Devices for Large-Scale Implementation of Associative and Temporal Sequence Learning, IEEE International Electron Devices Meeting, pp. 693-696, 2011 (hereinafter, Reference 3).
However, References 2 and 3 are intended to mimic the synapse by a memristor based device using a resistive switching material and a phase change material, respectively. These can mimic the long-term memory and the properties of the synaptic connections which are potentiated or depressed by the applying time differences of the pre- and post-synaptic signals. But, these cannot mimic the short-term memory that the stored information is naturally deleted within a short time period when the input signal temporarily disappears. Subsequently, these have a problem that the short-long term memory transition cannot be embodied.
And U.S Publication No. 2012/0084241A1 (hereinafter, Reference 4) is disclosed for techniques to mimic STDP properties that the synaptic connectivity connecting two neurons is changing by the spike time differences between pre- and post-synaptic neurons by using the phase change material as a synaptic device applied to the neuromorphic computation system. As like as References 2 and 3, since it uses the property of the phase change material, it cannot embody the property of the short-term memory of the biological synapse. Subsequently, it also has a problem that the short- and long-term memory transition cannot be embodied.